Literature summary for 4.2.1.3 extracted from

Cantu, D.; Schaack, J.; Patel, M.
Oxidative inactivation of mitochondrial aconitase results in iron and H2O2-mediated neurotoxicity in rat primary mesencephalic cultures (2009), PLoS ONE, 4, e7095.

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Localization

Localization	Comment	Organism	GeneOntology No.	Textmining

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	Q9ER34	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
midbrain	mitochondrial aconitase is over-expressed in primary mesencephalic cultures	Rattus norvegicus	-

Synonyms

Synonyms	Comment	Organism
aconitase	-	Rattus norvegicus

General Information

General Information	Comment	Organism
physiological function	it is investigated if oxidative inactivation of mitochondrial aconitase results in the release of redox-active iron and hydrogen peroxide and whether this contributes to cell death. Using an adenoviral construct mitochondrial aconitase is over-expressed in primary mesencephalic cultures. Oxidative inactivation of m-aconitase over-expressing cultures results in exacerbation of H2O2 production, Fe2+ accumulation and increased neuronal death. Increased cell death in m-aconitase overexpressing cultures is attenuated by addition of catalase and/or a cell permeable iron chelator suggesting that neuronal death occurred in part via astrocyte-derived H2O2	Rattus norvegicus

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Release 2023.1 (January 2023)